Terminal complement effectors in atypical hemolytic uremic syndrome: C5a, C5b-9, or a bit of both?
Kidney International, ISSN: 0085-2538, Vol: 96, Issue: 1, Page: 13-15
2019
- 8Citations
- 18Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations8
- Citation Indexes8
- CrossRef6
- Captures18
- Readers18
- 18
Article Description
The role of the terminal complement pathway as the cause of atypical hemolytic uremic syndrome (aHUS) is widely recognized, but the relative contribution of the effectors C5a/C5aR1 and C5b-9 to disease pathogenesis has not been defined. Using FH R/R mice carrying a factor H mutation that causes cell surface complement alternative pathway dysregulation, Ueda documented that in FH R/R mice, C5b-9 causes renal thrombotic microangiopathy (TMA) whereas C5a/C5aR drives macrovascular thrombosis. This commentary addresses the implications and limitations of this study.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0085253819303308; http://dx.doi.org/10.1016/j.kint.2019.02.038; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85067016844&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/31229026; https://linkinghub.elsevier.com/retrieve/pii/S0085253819303308; https://dx.doi.org/10.1016/j.kint.2019.02.038
Elsevier BV
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